Coronary heart disease is one of the leading causes of death in the United States. Heart attacks or myocardial infarctions caused by coronary heart disease can cause immediate death or can cause significant morbidity rates due to irreversible damage to the heart, such as scarring of the myocardial tissue.
Following a myocardial infarction there is always a certain time period of non-perfusion during which ischemia may develop. This is especially true during the patient transport to the hospital and until occluded vessels can be reopened by percutaneous transluminal coronary angioplasty (PTCA) or thrombolytic agents, for example. Thrombolytic agents, administered either intravenously or directly into the coronary arteries, work by dissolving the occluding thrombus and thereby reestablishing blood flow. When thrombolytic agents are administered properly, they can be expected to restore blood flow relatively quickly in cases of minor myocardial infarctions. However, in cases of massive myocardial infarctions, or in cases of delayed administration, the efficacy of the agents can be drastically reduced.
In situations where heart muscle damage has occurred due to myocardial infarctions or coronary heart disease, there have been attempts at improving perfusion in the damaged heart muscle and at repairing the heart muscle damage.
Some of the treatments have included attempts at growing microvessels through angiogenesis techniques. These techniques have experienced some significant drawbacks. The vessels that have been grown by these techniques have generally been too small in diameter and have provided little perfusion to the distant areas of the heart muscle, where perfusion is most needed. Also, most previous attempts such as U.S. Pat. No. 5,941,868 issued to Kaplan et al. involved injecting growth factors into the bloodstream in the target area which resulted in limited uptake into the heart muscle. These designs were at best only able to relieve symptoms of angina but provided no improvement of cardiac function and were not able to convert dead muscle area into working muscle.
Some of the treatments for revascularizing the myocardium have involved the creation of channels within the myocardium for providing oxygenated blood to myocardial cells without requiring coronary circulation.
U.S. Pat. No. 5,878,751 issued to Hussein et al. discloses stent and needle means for creating and maintaining a patent lumen in the diseased myocardium. The stent is carried into the myocardium through the heart wall on the outside of a needle and then the needle is withdrawn through the center of the stent.
U.S. Pat. No. 5,972,013 issued to Schmidt discloses a pericardial access device having a penetrating body axially mobile with the lumen of a guide tube. The guide tube includes a deflecting mechanism for deflecting the distal end of the penetrating body. In use, a patient's pericardium is contacted with the distal end of the guide tube and suction is applied to form a pericardial bleb. The penetrating body is axially mobilized distally within the lumen of the guide tube until the deflecting mechanism deflects the penetrating body to cause the penetrating end of the penetrating body to enter the bleb of the pericardial tissue at an angle oblique to the longitudinal axis of the guide tube.
Accordingly, what is needed is a catheter-based deployment system for introducing myocardial cellular materials into the heart wall in a minimally invasive procedure.